Oculomotor abnormalities identified in Huntington's disease (HD) and Parkinson's disease (PD) include defects in latency, saccadic velocity, and saccadic intrusions in smooth pursuit and fixation. The study of eye movement initiation has not been developed as yet in basal ganglia disease despite greatly expanded recent knowledge from non-human primate models. Specific neural circuitry has been mapped for mechanisms of supranuclear control involving basal ganglia, frontal eye fields, and superior colliculus by establishing the behavior-contingent conditions of neuronal discharge in these regions. We propose to apply these same sensitive testing paradigms to the analysis of initiation defects in pertinent human diseases of basal ganglia. Precisely timed initiation of eye movements is to be assessed in saccade latency tests to visual and to remembered stationary targets, and pursuit latency assessed to moving targets. We propose two additional measures are sensitive to impairment in initiation: a measure of the inhibition of inappropriate fixation to distracting stimuli, and a measure of the gain of smooth pursuit for tracking the initial 100 msec. "open-loop" segment of a pursuit initiating task. Because of the modulting influence of the basal ganglia structures and their projections on eye movement initiation in animals, we expect these test paradigms in humans will show disease-specific impairment patterns not previously described.